A Guide to Preclinical Models of Zoster-Associated Pain and Postherpetic Neuralgia

Warner, Benjamin E.; Goins, William F.; Kramer, Phillip R.; Kinchington, Paul R.

doi:10.1007/82_2021_240

Cited by 6 publications

(8 citation statements)

References 181 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…VZVspecific T cells persisting after HZ resolution may also aid host defense against future episodes of HZ in the same dermatome, as seen in murine studies with HSV, whereby local skin CD8 T RM provide anatomically restricted protection against reinfection 43 . Unfortunately, current animal models of VZV infection 44 are unlikely to contribute to functional studies of local VZV-specific T RM . Natural history investigations of local protection in human subjects against second episodes of HZ are also very challenging given the overall low incidence of recurrent HZ 19 .…”

Section: Discussionmentioning

confidence: 99%

Selective retention of virus-specific tissue-resident T cells in healed skin after recovery from herpes zoster

et al. 2022

View full text Add to dashboard Cite

Herpes zoster is a localized skin infection caused by reactivation of latent varicella-zoster virus. Tissue-resident T cells likely control skin infections. Zoster provides a unique opportunity to determine if focal reinfection of human skin boosts local or disseminated antigen-specific tissue-resident T cells. Here, we show virus-specific T cells are retained over one year in serial samples of rash site and contralateral unaffected skin of individuals recovered from zoster. Consistent with zoster resolution, viral DNA is largely undetectable on skin from day 90 and virus-specific B and T cells decline in blood. In skin, there is selective infiltration and long-term persistence of varicella-zoster virus-specific T cells in the rash site relative to the contralateral site. The skin T cell infiltrates express the canonical tissue-resident T cell markers CD69 and CD103. These findings show that zoster promotes spatially-restricted long-term retention of antigen-specific tissue-resident T cells in previously infected skin.

show abstract

Section: Discussionmentioning

confidence: 99%

Selective retention of virus-specific tissue-resident T cells in healed skin after recovery from herpes zoster

et al. 2022

View full text Add to dashboard Cite

show abstract

“…2 Newly synthesized virus particles are transported along the central and distal axons of all types of sensory neurons, which could lead to cell necrosis and apoptosis in the skin and DRG neurons. 3 Patients with HN show spontaneous pain, hyperalgesia, and abnormal pain sensitivity, 4 mostly moderate or severe pain, which has seriously affected the life quality of patients. 5 Besides, patients still suffer pain even several months after they healed from herpes, which is called postherpetic neuralgia (PHN).…”

Section: Introductionmentioning

confidence: 99%

“…During the onset of acute herpes zoster, the latent virus is activated, the virus begins to replicate and spread along the affected nerves, and finally triggers the inflammatory immune response that can damage peripheral and central neurons 2 . Newly synthesized virus particles are transported along the central and distal axons of all types of sensory neurons, which could lead to cell necrosis and apoptosis in the skin and DRG neurons 3 . Patients with HN show spontaneous pain, hyperalgesia, and abnormal pain sensitivity, 4 mostly moderate or severe pain, which has seriously affected the life quality of patients 5 .…”

Section: Introductionmentioning

confidence: 99%

HSV‐1 infection‐induced herpetic neuralgia involves a CCL5/CCR5‐mediated inflammation mechanism

Yang

et al. 2023

Journal of Medical Virology

View full text Add to dashboard Cite

Herpetic-related neuralgia (HN) caused by varicella-zoster virus (VZV) infection is one of the most typical and common neuropathic pain in the clinic. However, the potential mechanisms and therapeutic approaches for the prevention and treatment of HN are still unclear. This study aims to provide a comprehensive understanding of the molecular mechanisms and potential therapeutic targets of HN. We used an HSV-1 infection-induced HN mouse model and screened the differentially expressed genes (DEGs) in the DRG and spinal cord using an RNAseq technique. Moreover, bioinformatics methods were used to figure out the signaling pathways and expression regulation patterns of the DEGs enriched.In addition, quantitative real-time RT-PCR and western blot were carried out to further confirm the expression of DEGs. HSV-1 inoculation in mice resulted in mechanical allodynia, thermal hyperalgesia, and cold allodynia, following the infection of HSV-1 in both DRG and spinal cord. Besides, HSV-1 inoculation induced an up-regulation of ATF3, CGRP, and GAL in DRG and activation of astrocytes and microglia in the spinal cord. Moreover, 639 genes were upregulated, 249 genes were downregulated in DRG, whereas 534 genes were upregulated and 12 genes were downregulated in the spinal cord of mice 7 days after HSV-1 inoculation. GO and KEGG enrichment analysis suggested that immune responses and cytokine-cytokine receptor interaction are involved in DRG and spinal cord neurons in mice after HSV-1 infection. In addition, CCL5 and its receptor CCR5 were significantly upregulated in DRG and spinal cord upon HSV-1 infection in mice. And blockade of CCR5 exhibited a significant analgesic effect and suppressed the upregulation of inflammatory cytokines in DRG and spinal cord induced by HSV-1 infection in mice. HSV-1 infection-induced allodynia and hyperalgesia in mice through dysregulation of immune response and cytokine-cytokine receptor interaction mechanism. Blockade of CCR5 alleviated allodynia and hyperalgesia probably through the suppression of

show abstract

“…The pathology of PHN is still unknown. The persistent pain even after the clearance of the virus indicates a damage of the sensory nervous system 7 . Polymerase chain reaction analysis usually fails to detect HZ virus DNA in peripheral blood mononuclear cells of the PHN patients 8 .…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies also suggests that central sensitization plays a role in PHN 9 . Currently, the treatment of PHN relies on mitigating symptoms by addressing the chronic pain 7 . Early radical antiviral treatment of HZ could be helpful to prevent the progress of PHN.…”

Section: Introductionmentioning

confidence: 99%

Metabolomics profiling in predicting of post-herpetic neuralgia induced by varicella zoster

Lu,

Mei,

et al. 2023

Sci Rep

View full text Add to dashboard Cite

To explore potential metabolomics biomarkers in predicting post-herpetic neuralgia (PHN) induced by herpes zoster (HZ). A total of 90 eligible patients were prospectively enrolled and assigned into an acute pain (ACP) group and a PHN group. Serum samples were collected before clinical intervention to perform metabolomics profiling analyses using gas chromatography mass spectrometry (GC–MS). Key metabolites were identified using partial least squares discriminant analysis (PLS-DA). A binary logistic regression was used to build a combined biomarker model to predict PHN from ACP. The discriminating efficiency of the combined biomarker model was investigated and validated by internal validation. Six metabolites were identified as the key metabolites related to PHN. All these metabolites (N-Acetyl-5-hydroxytryptaMine, glucose, dehydroascorbic acid, isopropyl-beta-d-thiogalactopyranoside, 1,5-anhydro-d-sorbitol, and glutamic acid) were found elevated in the PHN group. Pathway analyses showed that glucose-alanine cycle, tryptophan metabolism, tyrosine metabolism, lactose degradation, malate-aspartate shuttle were top five metabolic pathways evolved in PHN. The AUC was 0.85 (95% CI 0.76–0.93) for the combined biomarker model, and was 0.91 (95% CI 0.84–1.00) for the internal validation data set to predict PHN. Metabolomics analyses of key metabolites could be used to predict PHN induced by HZ.

show abstract

A Guide to Preclinical Models of Zoster-Associated Pain and Postherpetic Neuralgia

Cited by 6 publications

References 181 publications

Selective retention of virus-specific tissue-resident T cells in healed skin after recovery from herpes zoster

Selective retention of virus-specific tissue-resident T cells in healed skin after recovery from herpes zoster

HSV‐1 infection‐induced herpetic neuralgia involves a CCL5/CCR5‐mediated inflammation mechanism

Metabolomics profiling in predicting of post-herpetic neuralgia induced by varicella zoster

Contact Info

Product

Resources

About